Advances in Neuropathic PainCME/CE

Philippe Vaillancourt, MD Rollin M. Gallagher, MD, MPH

Introduction

At the 25th Annual Scientific Meeting of the American Pain Society held in San Antonio, Texas (from May 3 to 6), 36 oral papers and 400 posters were presented covering pathophysiology, genetics, pain assessment, pharmacology and therapeutics, and interventional pain management as well as psychological, ethical, and legal issues pertaining to pain medicine. The meeting gathered physicians, psychologists, basic scientists, nurses, and other professionals interested in these issues. This review covers selected topics pertaining to neuropathic pain that were presented and discussed.

Sensitization Secondary to Spinal Cord Injury

S. Carlton,[1] of the University of Texas Medical Branch, Galveston, Texas, presented data on sensitization secondary to spinal cord injury. Using an injury model wherein a rat’s spinal cord is contused at T10, she showed that dorsal horn nuclei develop enhanced responses to peripheral stimulation not only at the thoracic level but also at the cervical level above. She recorded dorsal root reflexes in A delta and C fibers being stimulated in the dorsal horn by afferent nociceptors. Such stimulation results in antidromic volleys down sensory afferents causing neurogenic inflammation at the site of injury. This sensitization was blocked by intrathecal injection of the GABA antagonist bicuculline.

Carlton postulated that a reverberating central-peripheral nervous system loop is established following spinal cord injury. Following such injury, a “glutamate surge” is initiated, causing central sensitization of dorsal horn nuclei and the generation of dorsal root reflexes. This results in the peripheral release of neuropeptides and inflammatory mediators, which cause neurogenic inflammation and peripheral sensitization, and in turn cause central sensitization. These findings imply that mechanisms giving rise to central neuropathic pain are not exclusively central. In fact, peripheral nociceptors contribute to pain following a central injury. Peripheral targets or interventions may therefore be appropriate for treating chronic pain in that reduction of nociceptor activity reduces central and peripheral sensitization. This may help explain the conundrum of regionalization of central pain.

Gabapentin

Gabapentin exhibits variable absorption, a short half-life, and a ceiling of attainable blood levels. Backonja and colleagues,[2] in a randomized, double-blind, placebo-controlled study sponsored by the manufacturer, compared the gabapentin prodrug XP-13512 (XP) with regular gabapentin (Neurontin, Pfizer Inc., New York, NY) in 101 patients with postherpetic neuralgia. XP at two thirds the equivalent dose resulted in a 17% increase in the average plasma concentration of gabapentin compared with Neurontin. In the 36% of patients who had an increase in gabapentin average concentration greater than 30%, mean pain scores were significantly reduced compared with patients in the Neurontin group. Backonja and colleagues[2] concluded that improved gabapentin exposure afforded by XP may reduce pain in postherpetic neuralgia patients compared with Neurontin.

Fosphenytoin

Sang and colleagues,[3] from Brigham and Women’s Hospital in Boston, Massachusetts, evaluated the analgesic efficacy of fosphenytoin, a sodium channel blocker anticonvulsant, in patients with central neuropathic pain following spinal cord injury. They conducted a randomized, double-blind, placebo-controlled, crossover trial comparing a single 15-minute intravenous (IV) infusion of fosphenytoin 12-mg phenytoin equivalents (PE)/kg (the dose unit for fosphenytoin is expressed as a milligram equivalent of the phenytoin dose or “PE/kg”), fosphenytoin 4 mg PE/kg, lidocaine 2 mg/kg, and saline. Using a 21-point log-linear Gracely scale, they looked at the percentage of change from baseline in overall pain intensity. In the 12-mg PE/kg group, peak reduction in mean pain intensity was 50% at 45 minutes following the start of the infusion with a significant reduction compared with placebo over the entire 4-hour testing period. Trends were present but not statistically significant for the fosphenytoin 4-mg PE/kg and lidocaine 2-mg/kg groups. Fosphenytoin was well tolerated. It may well be that other sodium channel blockers in doses high enough to achieve significant serum levels may be effective in treating central neuropathic pain resulting from spinal cord injury.

Tapentadol

In a series of reports, Tzschentke and colleagues[4] and Terlinden and colleagues,[5] from Aachen, Germany, presented data on tapentadol, a new centrally acting analgesic with a dual mode of action: mu-opioid receptor agonism and inhibition of norepinephrine reuptake. The studies were all supported by the manufacturer Grunenthal GmbH. The drug was effective in a series of pain models in the rat, which included a sciatic nerve ligature model for neuropathic pain. Its potency was between that of morphine and tramadol. The drug achieved satisfactory serum levels after both IV and oral administration. It was generally well tolerated. The most common adverse effects associated with increasing IV tapentadol were sleepiness, vertigo, dry mouth, and nausea. Phase 3 clinical trials are planned for the near future in the United States. Tapentadol’s mu agonism and inhibition of norepinephrine reuptake make it similar to tramadol. However, tramadol consists of a racemic mixture of negative and positive enantiomers. The drug’s mu agonism depends on transformation of the positive enantiomer into an active “M-1” metabolite. The norepinephrine reuptake inhibition is mediated by the negative enantiomer. Tapentadol, on the other hand, requires no metabolism to be pharmacologically active. Both its mu-receptor agonism and norepinephrine reuptake inhibition are mediated by the same molecule. This may explain why its potency is higher than tramadol.

Lacosamide

Lacosamide is a drug under clinical development for the treatment of epilepsy and neuropathic pain by Schwarz BioSciences. In a multicenter, randomized, double-blind, placebo-controlled parallel group trial sponsored by the manufacturer, Kenney and colleagues[6] studied the effects of lacosamide at 200, 400, and 600 mg/day compared with placebo in a group of 469 subjects with painful distal diabetic neuropathy. In total, 33.6% to 68.2% of subjects across the groups completed the study, with the highest dropout rate occurring in the lacosamide 600-mg/day group. The incidence of side effects was also highest in this group. The primary variable was change in average daily pain score from baseline to the last 4 weeks of the maintenance phase on the basis of a 0-10 pain Likert scale. Secondary variables included assessment of pain at each visit with a 100-mm Visual Analog Scale, assessment of pain interference with sleep and activity, quality of life, and global impression of change in pain.

The change from baseline to the last 4 weeks of the maintenance phase in the Likert pain score (primary variable) was statistically significant in the lacosamide 400-mg group compared with placebo. Lacosamide 400 and 600 mg/day significantly reduced pain scores in patients with diabetic neuropathy during the entire titration and maintenance period as well as for the entire 18-week treatment period. Overall, 24.3% of patients dropped out of the trial on account of adverse effects. Lacosamide 400 mg was better tolerated than the 600-mg/day dose. Adverse effects appearing to possibly be dose-related included blurred vision (0% in the placebo group, 2.4% in the 400-mg group, and 5.1% in the 600-mg group), nausea (6.2%, 7.2%, and 18.2%, respectively), dizziness (4.6%, 21.6%, and 28.6%, respectively), tremor (0%, 9.6%, and 14.6%, respectively), somnolence (0%, 8%, and 8.8%, respectively), and imbalance (0%, 4.8%, and 9.5%, respectively).

Bicifadine

Bicifadine, a balanced inhibitor of norepinephrine and serotonin reuptake, was studied in 2 rat models of neuropathic pain by Basile and colleagues[7] in experiments supported by the manufacturer. Oral bicifadine suppressed both thermal and mechanical hyperalgesia in the Chung model of spinal nerve ligation-induced neuropathic pain with a duration of action of at least 4 hours. Mechanical allodynia in the Chung model was reduced with a maximum action at 40 mg/kg, an effect comparable to gabapentin 300 mg/kg. Mechanical hyperalgesia as measured in the streptozotocin-treated rat model of diabetic painful neuropathy was significantly inhibited by bicifadine. The drug is currently in phase 3 clinical development for the treatment of chronic low back pain with and without neuropathic symptoms.

Complex Regional Pain Syndrome

An interesting report of a patient with complex regional pain syndrome (CRPS) of both lower extremities treated with botulinum toxin was presented by Prager and Zerovich,[8] from UCLA. The patient was a 36-year-old woman who presented with the spontaneous onset of symptoms that were suggestive of CRPS in both legs. She responded for a finite period to antiepileptic drugs and tricyclic antidepressants. She then responded to lumbar sympathetic blockade at the L2 level with bupivicaine and triamcinolone, or bupivicaine and fentanyl for 1-3 weeks. A sympathetic block with 0.25% bupivicaine 15 mL and botulinum toxin type B 5000 units bilaterally resulted in 3 months of symptom relief. The blocks were repeated with botulinum toxin type A 50 units and bupivicaine 2.5 mL bilaterally at the L2 and L3 levels with similar results. In a personal communication, one investigator of this study reported similar results in a patient with CRPS of the upper extremity blocked with botulinum toxin combined with bupivicaine at the superior stellate ganglion. The presumed mechanism of action may be inhibition of acetylcholine exocytosis at the sympathetic ganglionic synapse. If these results can be replicated, sympathetic blockade with botulinum toxin may represent a significant improvement over a conventional block with anesthetic alone for the treatment of this often recalcitrant problem.

Conclusion

Neuropathic pain results from an affliction anywhere along the neuraxis from cortical neurons down to neurons in the anterior horn cell or in ganglia of the peripheral nervous system. Its causes include structural damage by disease, trauma, metabolic disturbance, and infection. It is often admixed with pain generated through stimulation of the peripheral pain receptors (nociceptive pain). It is frequently amplified by disordered mood. Increased understanding of its mechanisms, new drugs in the pipeline, new ways of using drugs that are already available, and novel interventional techniques, such as those described in this review, all contribute to the therapeutic armamentarium and allow us to chip away at the formidable nature of the problem.

References

Carlton S, Willis W, Jasmin L. Peripheral sensitization and inflammation: sensory nerves are a two way street. Program and abstracts of the 25th Annual Scientific Meeting of the American Pain Society; May 3-6, 2006; San Antonio, Texas. Oral Session 304.

Basile AS, Koustova E, Lippa A, Skolnick P. Bicifidine is an efficacious analgesic in animal models of neuropathic pain. Program and abstracts of the 25th Annual Scientific Meeting of the American Pain Society; May 3-6, 2006; San Antonio, Texas. Poster 667.

Prager J, Zirovich MD. Case report: use of botulinum toxin for sustained sympathetic blockade. Program and abstracts of the 25th Annual Scientific Meeting of the American Pain Society; May 3-6, 2006; San Antonio, Texas. Poster 791.

Anatomy of the Sacrum

A Word: Types of Arachnoiditis

Types of Arachnoiditis

The National Organisation for Rare Disorders (NORD) divides the condition thus:

Disorder Subdivisions

Adhesive Arachnoiditis

Arachnoiditis Ossificans

Neoplastic Arachnoiditis

Optochiasmatic Arachnoiditis

Postmyelographic Arachnoiditis

Rhinosinusogenic Cerebral Arachnoiditis

Spinal Ossifying Arachnoiditis

Under the International Classification of Diseases (ICD-9-CM) the following classification is used for arachnoiditis:

320 bacterial meningitis

321 meningitis due to other organisms

322 meningitis of unspecified cause

Arachnoiditis may be present in anyone who has had spinal injury, surgery or introduction of foreign substances, but in its most common form, arachnoid adhesions, tiny areas of scar material, it causes no clinically significant problems in the majority of patients.

The second type is local arachnoiditis, which generally results from some local insult to the subarachnoid space, such as injury or surgery.

This involves a larger, but still localised area of adhesions, which, again, may not cause symptoms.

However, this may constitute an undetected ‘time bomb’ which lurks for years and then precipitates symptoms suddenly apparently out of the blue after a seemingly innocuous event such as a fall or minor car accident.

The exact reason for the sudden sustained exacerbation of symptoms and sometimes decline is not known, although it may be due to bleeding into the CSF, with subsequent inflammation and proliferation of scar tissue, to the extent that nerve roots become sufficiently compromised to precipitate overt clinical symptoms and signs.

The most severe type, which is more likely to cause symptoms, is adhesive arachnoiditis.

This can be mild, moderate or severe, and either focal (localised) or diffuse. The latter type tends to result from insults involving introduction of foreign substances into the subarachnoid space.

It may rarely be progressive. In adhesive arachnoiditis arising due to injections into the spinal fluid, (chemically-induced adhesive arachnoiditis), the more widespread damage may also be associated with systemic symptoms.

Spinal adhesive arachnoiditis may be localized: at one vertebral level segmental: in two or more levels within a spinal region e.g. lumbar contiguous: in two or more adjacent vertebral levels diffuse: if spread over more than one spinal region e.g. lumbar and thoracic.

In the 1999 Global survey, I found the following levels of lesions:

Lumbar: 87%

Thoracic: 23%

Cervical: 34%

Cranial: 14% of which brainstem 1 case

Widespread (more than 1 level): 91 cases of which 23 had cranial involvement;

45% of respondents who had undergone an oil-based myelogram had widespread arachnoiditis; compared with 21% of those who had had a water-based myelogram, 27% of those who had unspecified dye, and 8% of those who had had an epidural injection of some kind.

Pachymeningitis

Aldrete ([i]) contends that pachymeningitis is “probably one of the most severe advanced anatomopathological phases” of arachnoiditis, being characterised by proliferation of scar tissue to the extent of encasing the spinal cord and nerve roots.

Pachymeningitis affects the dural layer of the meninges.

Wilson ([ii]) suggested that the subdural space reacts to the insult of an irritant by producing a well-organised, laminar (layered) fibrosis that resembles a healing subdural haematoma.

Arachnoiditis in the cauda equina can cause a chronic cauda equina syndrome.

This involves pain and sensory disturbance and weakness in the lower limbs, with saddle anaesthesia and bladder, bowel and sexual dysfunction.

A rat study ([iii]) demonstrated the deleterious effects that cauda equina adhesions have upon supply of nutrients to the nerve roots: in complete cauda equina adhesion, the glucose transport to the cauda equina from the cerebrospinal fluid was reduced by 72% compared with the normal cauda equina.

The authors concluded:

“Considering the greater nutritional importance of the cerebrospinal fluid in the cauda equina, it is most likely that the impairment of nutritional supply to adhered cauda equina may lead to eventual neural degeneration.”

If the spinal cord is affected, there may be areas of ischaemic damage, myelomalacia (softening of the tissue) and formation of cysts.

Perineural Tarlov cysts located on lumbo-sacral roots can be a cause of cauda equina syndrome.

OBJECTIVES:
1) To draw attention to the fact that multiple Tarlov lumbo-sacral perineural cysts can produce serious movement disturbances.
2) To document the usefulness of the magnetic resonance imaging in noninvasive diagnosis of perineural cysts.

CASE DESCRIPTION: A male patient, 80 years of age, suffered from progressive weakness of lower limbs, which caused an increasing drop of the feet. The disease began in August 2000, following a long journey by train. The patient additionally complained of urinary incontinence as result of sneezing, coughing or fast walking. The urologist did not find prostatic gland hypertrophy. An examination by the internist revealed atheromatous myocardiopathy in circulation failure stage. Magnetic resonance imaging showed multiple perineural cysts up to 15 mm in diameter on lumbo-sacral roots. This clinical picture, supported by the magnetic resonance imaging allowed to recognize cauda equina syndrome caused by Tarlov lumbo-sacral perineural cysts.

DISCUSSION: This case is a reminder, that part of perineural cysts, particularly multiple, can be a cause of nerve roots injury, and their lumbo-sacral location can produce cauda equina syndrome. As reported by Zarski and Leo, Tarlov cysts were cause of 7.3% of pain syndrome cases 2 patients in the study group showed lower limb claudication. Magnetic resonance imaging of patients with back pain, performed by Paulsen, Call and Murtagh, revealed that Tarlov cysts occurred in 4.6% of patients, but only 1% had the symptoms connected with the presence of those cysts. In available Polish literature no report has been found referring to fixed cauda equina syndrome which was caused by multiple cysts revealed through the magnetic resonance imaging of spinal canal. Only Zarski and Leo, discussing the correlation between the clinical and radicographic picture, described transient cauda equina syndrome in two patients who, beside Tarlov cysts, were also found to have intervertebral lumbosacral disc herniation. Tarlov was the first to describe well documented cauda equina syndromes caused by cysts on the lumbo-sacral roots. It is necessary to emphasize the established role of magnetic resonance of spinal canal in the diagnosis of perineural cysts on the lumbo-sacral roots as well as other anatomical anomalies of cerebrospinal fluid spaces. Despite the fact that cauda equina syndrome in the case reported here was a serious complication of multiple Tarlov cysts in the lumbo-sacral region, a surgical treatment was not undertaken; in such cases this treatment should be the chosen procedure.

NERVE BLOCKS 101

What are blocks?

Blocks are injections of medication onto or near nerves. The medications that are injected include local anesthetics, steroids, and opioids. In some cases of severe pain it is even necessary to destroy a nerve with injections of phenol, pure ethanol, or by using needles that freeze or heat the nerves. Injections into joints are also referred to as blocks. Although not technically correct, such “shorthand” is commonly used.

1. Blocks with local anesthetic can be used to control acute pain. (Hence, the shot at the dentist or the epidural block for a surgery or a delivery.)

2. Pain and injury often makes nerves more sensitive, so that they signal pain with less provocation. Think about lightly brushing against your skin when you have a sunburn. Blocks can provide periods of dramatic pain relief, which promotes the desensitization of sensory pathways.

3. Steroids can help reduce nerve and joint inflammation and can reduce the abnormal triggering of signals from injured nerves.

4. Blocks often provide diagnostic information, helping to determine the source of the pain.

Remember, blocks are not the best treatment for all pain problems.

Spinal Injections:

The most common spinal injection is the lumbar epidural steroid injection. This is particularly useful for pain that radiates from the lower back into a leg, and is caused by disc herniation or spinal stenosis (narrowing around the nerves) which triggers nerve root irritation. Similar injections can be very useful in the cervical spine, where the symptoms will extend into the arms. Thoracic epidural steroid injections are most commonly used to reduce the pain associated with herpes zoster (shingles). Such blocks may reduce the risk of developing persistent postherpetic neuralgia (i.e., pain which persists long after the skin eruption has healed).

The facet joints of the spine can also cause pain. Injections into the facet joints or blocks of the nerves that go to the facets can often be very helpful with these pains. This problem is more common in the lumbar spine, but also occurs in the neck.

Discograms (intradiscal injections of contrast under fluoroscopy or CT imaging) can determine if and which disc is the source of the pain. This can help a surgeon determine which levels of the spine require surgery. If the patient is found to have a painful disc, they may be a candidate for a new and promising technique, intradiscal electrothermoplasty (IDET). In a procedure similar to a discogram, a wire is temporarily inserted into the disc and used to heat the disc. This destroys the invading sensory nerves and causes the proteins of the disc wall to reshape and slowly strengthen (over 3-6 months). The procedure cannot be done if the disc has already severely degenerated.

Spinal Cord Stimulator Questions to Ask

If your chronic pain has not responded to a progressive plan of pain management (the chronic pain treatment steps), spinal cord stimulation (SCS) may be an option. An open and honest talk with your physician will help to determine if you are a good candidate for this treatment option.

Spinal cord stimulation works best for unresolved neuropathic pain in the trunk and/or limbs. It is unlikely that spinal cord stimulation will relieve nociceptive pain. Ask your physician if the cause, type, and location of your pain make you a candidate for spinal cord stimulation.

Remember, in the context of the chronic pain treatment steps, spinal cord stimulation is an advanced pain treatment. This means that spinal cord stimulation is generally not considered a treatment option until other pain therapies including analgesics, NSAIDs, nerve blocks, and perhaps even surgery have been tried and have failed to control your pain.

What is your experience with spinal cord stimulation?

Ask about your physician’s clinical experience with spinal cord stimulation. Has he or she prescribed spinal cord stimulation for other patients? What kind of pain conditions did they have and what type of system did he or she prescribe for them? Did spinal cord stimulation provide good outcomes for these patients? If yes, what made spinal cord stimulation therapy successful? If no, was there a common factor that contributed to the therapy’s lack of success? Are there patients I can talk to who had similar pain complaints and have undergone SCS therapy? Does the physician have an SCS patient I can talk to?

Some physicians may be familiar with spinal cord stimulation but do not have direct experience with it. If this is the case and you are a potential candidate for spinal cord stimulation therapy, your physician may refer you to a pain specialist for treatment and evaluation, or your health plan may permit you to visit other physicians without a referral.Are you recommending an implantable pulse generator (IPG), rechargeable IPG, or a radio-frequency (RF) spinal cord stimulator?

Each type of system has advantages and disadvantages. The decision should be based on the pattern and complexity of your pain, your lifestyle, and how much electrical energy will be required to give you adequate pain relief.

If an IPG system is being recommended, ask

How likely is it that my pain will worsen or spread over time?

If my pain pattern were to spread or worsen over time, would the IPG still be capable of providing sufficient coverage?

Is the IPG’s power capacity and programming capabilities sufficient to provide complete stimulation coverage of all painful areas?

How often will the IPG need to be replaced?

What does the procedure for IPG replacement entail?

If a rechargeable IPG system is being recommended, ask

Will the system ever need to be replaced?

Based on my power requirements, how often will I need to recharge the system?

How long does it take to recharge the system?

How long does it take to recharge the system?

Are there any safety issues related to recharging?

Can the system die if not recharged regularly?

What is the procedure for replacing a rechargeable IPG system?

If an RF system is being recommended, ask

If my pain changes or spreads, what are my options?

Is the RF system’s power capacity and programming capabilities sufficient to provide complete stimulation coverage of all painful areas?

How do patients with RF systems incorporate the transmitter into their daily attire?

Can I see the RF system components? Seeing the antenna and transmitter may help you make your decision.

During the trial period, will I be able to test the IPG, rechargeable IPG, and RF programs?

A trial implantation is one of the most important ways to determine if spinal cord stimulation therapy will give you enough pain relief.

A multi-program trial takes this degree one step further. A multi-program trial not only allows you to test if spinal cord stimulation is effective, but it also allows you to see which type of system IPG, rechargeable IPG, or RF might be best for your situation.

A multi-program trial involves placing several stimulation programs into a trial spinal cord stimulator. These programs can recreate the stimulation provided by an IPG, rechargeable IPG, or RF system. By recreating these systems, you can try the features of each to see which one provides the greatest pain relief. It also gives you an idea of which system is more appropriate in terms of the power requirements you need to attain sufficient pain relief.

A multi-program trial is an important advantage when considering stimulation systems. It can help ensure that you receive a stimulator capable of the providing you with the greatest level of pain relief, both now and over time.

When you talk with your physician about the trial, ask

How do you determine if an IPG, rechargeable IPG, or RF system is best?

Will you conduct a multi-program trial that allows me to test the IPG, Rechargeable IPG, and RF systems?

What type of lead and how many electrodes will you implant during the trial? Do you use extra electrodes in order to cope with pain or leads that move?

How long does the trial last? Under what circumstances would you extend or shorten the trial?

If the stimulation is not very effective in providing pain relief, will you reprogram the system and extend the trial or choose to remove the system?

If the trial is successful, how soon will the permanent system be implanted?

Will you involve me in the decision about which permanent system will be implanted?

What are the programming features of the system that will be implanted?

Programmability is one of the most important features of a spinal cord stimulator. The greater the programmability, the greater the likelihood that the system can provide you with enough pain relief. A spinal cord stimulator with extra programming features is more adaptable if your pain relief needs change over time.

Your physician should want to implant the system that offers the greatest chance for success. You can better discuss this with your physician by knowing about the features and capabilities of the IPG, rechargeable IPG, and RF systems that are currently available.

When discussing the systems, ask your physician

Which type and model of stimulator do you recommend and why?

If an IPG is being considered, can you estimate the amount of energy required to achieve enough pain relief for my pain condition and how long the battery will last?

If a rechargeable IPG is being considered, how often will the system need to be recharged? How long does this recharging usually take? How much time will pass before I need to recharge again?

What type of lead and how many electrodes will you implant? Will you place more electrodes than what might be currently necessary in case my pain pattern or the location of my pain changes in the future?

Are there any safety issues with certain systems?

What is the system’s capability for electronically repositioning the lead(s) using the external programmer/transmitter?

How many of your patients with this type of system have had another surgery to reposition their leads?

How many and what type of stimulation programs does the system offer? If only one or two, is this enough to cover my pain pattern?

Does a system that offers more stimulation programs offer greater control over my pain therapy and increase my chances for success over the long-term?

Will I be able to manually select stimulation programs stored in the system, or does changing programs require an office visit?

Can I help choose the system to be implanted?

It takes a team effort to get a good outcome with spinal cord stimulation (defined as a decrease in pain of 50 percent or more). Your physician and/or his or her staff or a representative will program your spinal cord stimulator and teach you how to use it. But from that point on, success depends on your willingness to participate fully in your therapy.

You can start by asking your physician

What can I do to improve my chances for success?

How long will it take me to heal after the implantation surgery?

Do I have to restrict physical activities? For how long?

How often will I return for follow-up visits?

When can I get back to interests and activities?

What have other patients done during and after their recovery that made a difference in their outcomes?

Taking charge of your therapy is the first step to recovery and a world of new possibilities for a better quality of life.

BOSTON – April 2, 2004 – Researchers from Massachusetts General Hospital (MGH) have found physical evidence of a previously unknown communication between nerves on opposite sides of the body. In the May 2004 issue of Annals of Neurology, the scientists describe how cutting a major nerve in one paw of a group of rats resulted in a significant decrease in skin nerve endings in the corresponding area of the opposite limb. The study, released on the journal’s website, may have major implications for the care of patients with nerve damage and also calls into question the common practice of using tissues on the opposite side of the body as controls in scientific experiments.

“Patients with pain syndromes related to nerve damage sometimes report symptoms on the side opposite their injury as well, but those reports are usually discounted because there has been no biological framework for the phenomenon,” says Anne Louise Oaklander, MD, PhD, director of the MGH Nerve Injury Unit, the report’s principal author. “Our evidence means that these reports can no longer be ignored and gives us a new direction for research.”

It has been known for more than 100 years that, when a nerve is cut, skin nerve endings in the area supplied by that nerve quickly disappear. This is because nerve cell bodies are actually located near the spinal cord, and nerve fibers called axons extend into the limbs. When axons are severed, downstream nerve endings are cut off from the cell body and die.

Reports of opposite-side sensory effects of injury date back to the American Civil War. However, no connections are known to exist between nerve cells supplying corresponding areas on the left and right sides. In previous research Oaklander and her colleagues examined nerve endings in patients with post-herpetic neuralgia – persistent pain in an area of skin previously affected by shingles, also called herpes zoster. Along with an almost total loss of nerve endings at the site of the shingles outbreak, they also found that almost half the nerve endings on the opposite side skin had been lost, even though patients did not report pain on that side. But since shingles is caused by the varicella zoster virus, which also causes chicken pox, there was a possibility that the damage had been caused by viral spread through the spinal cord.

In the current study, Oaklander and her co-author Jennifer Brown describe their experiment in three groups of rats – an experimental group in which the tibial branch of the sciatic nerve was cut in one hind paw and two control groups, one which had sham surgery and the other had no procedures. Within one week of injury, rats in the experimental group lost almost all skin nerve endings in the part of the paw supplied by the tibial nerve. Surprisingly, they also lost 54 percent of nerve endings in the corresponding area in the opposite paw. No changes were seen in either control group. The researchers also examined the opposite-limb-area supplied by the uncut nearby sural branch of the sciatic nerve and found no change in nerve endings.

“This loss of nerve fibers in the contralateral limb is so precise – being confined to areas innervated by the matching nerve – that the communication is likely to involve nerve cells or the supporting glial cells,” says Oaklander, an assistant professor of Anesthesia and Neurology at Harvard Medical School. “We need to look into what regulates this communication and how it may be altered to help treat nerve injury and pain patients.”

Massachusetts General Hospital, established in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $400 million and major research centers in AIDS, cardiovascular research, cancer, cutaneous biology, medical imaging, neurodegenerative disorders, transplantation biology and photomedicine. In 1994, MGH and Brigham and Women’s Hospital joined to form Partners HealthCare System, an integrated health care delivery system comprising the two academic medical centers, specialty and community hospitals, a network of physician groups, and nonacute and home health services.

Surgical Management of Arachnoid Cysts with Autogenous Fat Grafts

This is the book cover of the classic 1971 publication by neurosurgeon Isadore Tarlov on the subject of sacral nerve root cysts. Initially Tarlov thought that these cysts were always benign but it soon became known by clinicians that, in some cases, these cysts were capable of becoming another important cause of the “Sciatic or Cauda Equina Syndrome”.

When sacral nerve root cysts increase in size and internal tension to the point where they actually erode adjacent bone they require surgical intervention. Present options for treatment vary. A recent neurosurgical paper advocated shunting these cysts to the abdomen. With respect to William of Occam’s Razor the Editor is pleased to present a series of examples of sacral nerve root (Tarlov) cysts treated effectively by other means.

In order to fully appreciate the series of cases being presented one needs to recognize the fact that a typical “Tarlov Nerve Root Cyst” is only an interesting finding on an MRI scan, having no clinical significance . An example of this is shown (incidental finding) on a routine MRI scan. The red dot identifies the cyst.Since Tarlov’s pioneering work it has been recognized that the sometimes tenuous communication of these congenital cysts to the subarachnoid space (and the cerebrospinal fluid) can become partially or completely occluded. When partially occluded (usually due to the obstruction produced by proteinaceous material) a “ball valve” phenomenon can occur where fluid can enter and not leave. In such events the tension within the cysts gradually increases producing erosion of surrounding bone and compression of local nerves.

These images show the case of a 48 year old female who was progressively incapacitated by leg pain and numbness. In addition to a large sacral cyst eroding the sacrum the nerve roots (shown with a green dot) were clumped together from local adhesive arachnoiditis. The surgical view shows the opened cyst. Autogenous, soft, fat grafts, were used to fill the defect. Following decompression the patient experienced immediate relief of all symptoms. The image to the left shows a post-operative CT scan with a label over the fat graft.

Immediately above is another case of a large sacral cyst (red dot) extending from L5-S3 and eroding bone. The surgical view of the opened cyst reveals nerve roots adherent to the dura demonstrating adhesive arachnoiditis. This patient was also successfully treated with an autogenous fat graft.

The following series of cases show progressively more severe cases of clinically significant arachnoidal cysts. In the case to the left erosion of the sacrum has just begun.

Here a prominent cyst complex is evident. In the saggital view it the cyst has extended itself through the anterior sacrum into the retroperitoneal space.

In this example the bone destruction has been so great that the stability of the sacrum itself has become a matter of concern.

The Burton Experience, over the years, in treating clinically significant sacral nerve root cyst problems, over the years, has conformed that appropriate fat grafting techniques are the most effective in dealing with these entities. Other treatment modalities often create more problems than they solve.

An example of this is the case shown to the left where a fibrin glue was injected into the cyst (red dot). This glue is now adherent to the nerve roots and any attempted surgical dissection runs the high risk of associated nerve injury.

UNDERSTANDING SCIATICA

Low back pain and/or leg pain that usually travels down the large sciatic nerve, from the lower back down the back of each leg, is generally referred to as sciatica and is fairly common. This pain can be caused when a nerve root in the lower spine that helps form the sciatic nerve is pinched or irritated.

Sciatica is usually caused by pressure on the sciatic nerve from a herniated disc (also referred to as a ruptured disc, pinched nerve, slipped disk, etc.) in the lumbar spine. The problem is often diagnosed as a “radiculopathy“, meaning that a disc has protruded from its normal position in the vertebral column and is putting pressure on the radicular nerve (nerve root) in the lower back, which forms part of the sciatic nerve.

Sciatica occurs most frequently in people between 30 and 50 years of age. Often a particular event or injury does not cause sciatica, but rather it may develop as a result of general wear and tear on the structures of the lower spine. The vast majority of people who experience sciatica get better with time (usually a few weeks or months) and find pain relief with non-surgical treatments.

Practical point:Symptoms of sciatica pain can vary greatly but usually decreases after a few weeks or months with non-surgical treatment.

Understanding sciatica pain
For some people, the pain from sciatica can be severe and debilitating. For others, the pain might be infrequent and irritating, but has the potential to get worse. Usually, sciatica only affects one side of the lower body, and the pain often radiates from the lower back all the way through the back of the thigh and down through the leg. Depending on where the sciatic nerve is affected, the pain may also radiate to the foot or toes.

One or more of the following sensations may occur as a result of sciatica:

Pain in the rear or leg that is worse when sitting

Burning or tingling down the leg

Weakness, numbness or difficulty moving the leg or foot

A constant pain on one side of the rear

A shooting pain that makes it difficult to stand up

Low back pain may be present along with the leg pain, but usually the low back pain is less severe than the leg pain

While sciatica can be very painful, it is rare that permanent nerve damage (tissue damage) will result. Most sciatica pain syndromes result from inflammation and will get better within two weeks to a few months. Also, because the spinal cord is not present in the lower (lumbar) spine, a herniated disc in this area of the anatomy does not present a danger of paralysis.

Symptoms that may constitute a medical emergency include progressive weakness in the leg or bladder/bowel incontinence. Patients with these symptoms may have cauda equina syndrome and should seek immediate medical attention. In general, patients with complicating factors should contact their doctor if sciatica occurs, including people who: have been diagnosed with cancer; take steroid medication; abuse drugs; have unexplained, significant weight low; or have HIV.

Any condition that causes irritation or impingement on the sciatic nerve can cause the pain associated with sciatica. The most common cause is a lumbar herniated disc. Other common causes of sciatica include lumbar spinal stenosis, degenerative disc disease, or isthmic spondylolisthesis.

Sciatica medical definition
To clarify medical terminology, the term sciatica (often misspelled as ciatica or siatica) is often used very broadly to describe any form of pain that radiates into the leg. However, this is not technically correct. True sciatica occurs when the sciatic nerve is pinched or irritated and the pain along the sciatic nerve is caused by this nerve (radicular pain). When the pain is referred to the leg from a joint problem (called referred pain), using the term sciatica is not technically correct. This type of referred pain (e.g. from arthritis or other joint problems) is quite common.

Sciatica treatments
Sciatica nerve pain is caused by a combination of pressure and inflammation on the nerve root, and treatment is centered on relieving both of these factors. Typical sciatica treatments include:

Non-surgical sciatica treatments, which may include one or a combination of medical treatments and alternative (non-medical) treatments, and almost always includes some form of exercise and stretching. The goals of non-surgical treatments should include both relief of sciatica pain and prevention of future sciatica problems.

Sciatica surgery, such as microdiscectomy or lumbar laminectomy and discectomy, to remove the portion of the disc that is irritating the nerve root. this surgery is designed to help relieve both the pressure and inflammation and may be warranted if the sciatic nerve pain is severe and has not been relieved with appropriate manual or medical treatments.

Tethered Cords

This term describes a range of signs and symptoms consequent to the tethering of a spinal cord at any level. It is often associated with spina bifida occulta and spinal dysraphism. It is diagnosed after an investigation of the embryology, pathophysiology and clinical symptoms using diagnostic neuro-imaging, and examination and observation of the patient. It is “classically defined as having the tip of the [spinal] cord below the L2 vertebra instead of at the L1-L2 disc space level” [Selcuki and Coskun, 1998]. Tethered spinal cords are non-life-threatening congenital conditions, but the consequences of not recognising, not monitoring, and in most cases not correcting, them can be deformed feet and legs, progressive neurological impairment, and, at worst, paralysis and incontinence, depending on the severity and type of cord tethering.

Normal spinal cordThe normal spinal cord begins at the junction of the skull with the cervical (neck) spine, and the cord continues down the spinal column until the mid-back region, the lumbar area. Beyond this point nerves continue down the spinal canal (as the cauda equina) and the spinal cord ends with the non-functioning tissue known as the filum terminale, which usually has the elasticity similar to a rubber band. The cord and the spinal bones (vertebrae) initially start out the same length but as the foetus and child grows, the vertebrae grow faster than the cord and therefore the cord effectively “ascends” within the spinal column. In people with no tethered cord the spinal cord ends up hanging freely within the vertebrae, protected by cerebrospinal fluid and, as there is no obstruction to its movement, it is able to flex and move freely with everyday activities.

I had reservations about including all the following details in this section, but it may help to explain the embryology and creation of tethered cords.
(Source of information: http://www.yoursurgery.com/ ).

A tethered spinal cord is characterised by an abnormal attachment of the distal spinal cord to the surrounding tissues. The lower end of a normal spinal cord is found in the upper lumbar spinal canal. The attachment to the spinal canal or bones usually causes the spinal cord to end lower in the lumbar or sacral spinal canal. In the majority of cases, it is congenital (the patient is born with it).

Developmental Anatomy

In the developing foetus the spinal cord is formed by a complex process. It forms from the same layer of cells that later forms the skin (called the ectoderm)

Beginning around the 18th day of development and extending to the 22nd day, the spinal cord is formed by a process called neurulation

1. The ectodermal layer thickens in the midline of the back forming neuroectoderm that first forms a groove and then a tube that drops below the surface to be later protected by bone and muscle

2. As the tube drops below the surface, skin closes over the tube

3. The tube begins to close first in the thoracic (chest) region and the closure spreads toward the head (to eventually form the brain) and towards the upper lumbar region

The lowest part of the spinal cord is formed by a different process called canalization and caudal regression during the 28-48th day of development

1. A group of ectodermal cells lying beneath the skin’s surface at the primitive “tail” begins to break down in its centre to form a neural tube (canalization)

2. This tube then fuses with the neural tube formed by neurulation

3. This distal spinal cord degenerates to form the filum terminale

4. This process is less precise and therefore more liable to defects than neurulation. Failure of degeneration creates the entity of tight filum terminale

Beginning about the 45th day, a third process called regression occurs and extends into the first year of life

1. The lower neural tube then forms into the lowest part of the spinal cord (conus medullaris), the nerve roots that go to form the nerves to the legs (cauda equinae) and a fibrous cord from the conus medullaris (filum terminale)

2. By the process of regression and a greater growth of the bony spine than the spinal cord, the conus medullaris eventually ends up at the level of the second lumbar vertebrae.

Pathology

Any event which interferes with the development of the spinal cord and cauda equinae can lead to the ingrowth of other tissues like fat and skin, which creates an abnormal attachment, or tethering of the spinal cord

Tethering of the spinal cord interferes with the normal regression process causing damage to the spinal cord as it is stretched and placed under abnormal tension

The tension injures the spinal cord and may cause symptoms

Other entities can be associated with tethering including tumours, cysts, tracts and spinal cord malformations. There are several distinct entities forming a spectrum of diseases, some of which are listed below. The skin over the tether is intact and usually the surrounding bone of the spine is incomplete (spina bifida occulta). This is also called an occult spinal dysraphism (OSD)

Dermal sinus: A tract lined by skin cells that leads from the skin to anywhere along the back of the spine

Lipoma or lipomyelomeningocele: malformations in which a fatty tumour under the skin is fused to the back of the lower spinal cord

Epidermoid or dermoid cyst: similar in formation to a dermal sinus, but a benign tumour is formed somewhere along the tract

Diastematomyelia (split cord malformation): usually involves the upper portion of the cord. The spinal cord is split in two by a bony spur

Tight filum terminale syndrome: a thickened filum over 2mm in diameter, a low lying conus medullaris and no other cause of tethering

Neurenteric cyst: a cyst lined by tissue similar to the gut or airway. It has a connection to the spinal cord, vertebrae or both. The spinal tumour may connect via a stalk to the gut

Myelocystocele: a complex malformation in which the end of the spinal cord is ballooned into a cyst and is associated with syringomyelia

Syringomyelia: dilatation of the central portion of the spinal cord.

Retether following myelomeningocele repair: after a SB repair, the spinal cord may become tethered by scarring to the area of repair

Tethered spinal cord

The embryonic spinal bones fuse together at different rates in a zip-like fashion proceeding in both directions. However, the bones at the caudal (tail) end form by coalescing in a disorganised way, and if the spinal cord becomes trapped in this area of rapidly amassing material, it becomes “tethered”. Due to tethering, as the child grows there is no free movement of the cord and it is not able to ascend the spinal column. The lower part of the cord is therefore stretched and progressive neurological damage occurs as more tension is placed on the nerves emanating from the end of the cord. Blood circulation to the cord and the lower extremities may be reduced and in most cases the nerve impulses may be weak, distorted or absent.

Schneider et al (in Tethered Cord Syndrome, edited by Shokei Yamada, published by the American Association of Neurosurgeons Publications Committee, 1996) showed that blood flow was lowered during tethering but was significantly increased after detethering.

Neuronal (nerve) dysfunction due to tethering is subsequent to, firstly, metabolic derangement or hypoxia (the reduction of oxygen supply to tissues below physiological levels, despite adequate passage of blood through the tissue), and, secondly, the electrophysiology of the cord is impaired due to the distortion of neuronal membranes. Effectively, hypoxia means that the cord is deprived of oxygen and therefore electrical impulses are depressed. Physically this causes the nerves to reduce or stop sending impulses, both for sensory and motor functions, thereby creating and exacerbating progressive neurological deterioration.

At birth, there may be few external signs that the cord is tethered and as the spinal cord and its tissues are generally not fully exposed, there is rarely cause to operate immediately, except perhaps in the case of connecting dermal sinus tracts (skin-to-cord). A lipomyelomeningocele is most obviously visible as a skin-covered fatty mass in the lumbosacral region.

It used to be thought that most of the nerve stretching occurs at a time of rapid growth at puberty, but foot deformities and scoliosis can be apparent by the age of two as the cord stretching has effectively been going on since ~ 6 weeks post-conception. Once damaged, neurological function may not necessarily be recovered or improved. As indicated in the sections on spinal dysraphism, both children and adults can experience worsening symptoms of tethered spinal cords. In children the deterioration is caused by stretching of the cord with natural childhood growth. However in adults “without appropriate intervention most deteriorations in tethered cords are gradual, insidious over years. Rarely it can be very sudden, as can occur if one is put in the lithotomy position. Irreversability also occurs slowly and insidiously”. [Ian Pople, 2002]. Also see this article by Shokei Yamada, which is very informative: “Pathophysiology of Tethered Cord Syndrome: Correlation with Symptomatology”, Neurosurgical Focus, 16(2), 2004, Article 6

Adults with prior stable symptoms of a tethered cord can experience worsening of their symptoms due to general physical wear and tear on the cord and spinal nerves, and subsequent hypoxia and ischaemia of the spinal cord. These symptoms may be increased pain, decreased function, mobility and sensation, and further deformation of already poor feet. They may be fully accustomed to their condition, but any new symptoms that are out of the ordinary should be investigated by neurosurgical consultants who have a special interest in the area of spina bifida and spinal cord tethering. Surgery may be recommended in order to arrest further neurological damage and the deterioration of the function and sensation of the limbs, bladder and bowel.

In Journal of Neurosurgery, April 2001, 94(2 Suppl), the authors R. van Leeuwen, N.C. Notermans and W.P. Vandertop addressed the issue of “Surgery in Adults with Tethered Cord Syndrome: An Outcome Study with Independent Clinical Review”. The abstract is below:

“Object: The authors conducted a study to evaluate the risks and short-term benefits of surgical treatment for tethered cord syndrome (TCS) in patients older than 18 years of age.

Methods: The authors studied a series of 57 consecutive adult patients with TCS of varying origins. Patients were examined by the same neurologist in a standard fashion before and after surgery, and most were followed for at least 2 years post-operatively. The patients’ ages ranged from 19 to 75 years. The mean age at onset of symptoms and diagnosis was 30 years and 37 years respectively. Muscle strength improved (15 cases) or showed no change post-operatively (38 cases) in a large majority of patients (93%). In four patients a minor decrease in muscle strength was demonstrated, and there was a significant deterioration in two (3.5%). In the two latter patients a rapid decline in motor function was present pre-operatively. Subjective assessment of pain, gait, sensory function, and bladder/bowel function at 4 weeks, 6 months and 2 years post-surgery revealed improvement in a substantial percentage of patients. No major surgery-related complications occurred.

Conclusions: This is the largest series to date in which adult patients with TCS comprise the report. Untethering procedures in these patients were safe and effective, at least in the short term. Patients with rapid loss of motor function, lipomyelomeningocele, or split cord malformation seem to be at a higher risk of post-surgery deterioration. A follow-up period of many more years will be necessary to determine whether aggressive surgery is beneficial in the long term.”

Click here for a very informative medical site on tethered cords. It includes images (not too gory!) and text describing symptoms and causes of tethered cords, and is easy to read and understand.

There are four main forms of tethered spinal cord in the spina bifida occulta range.

The following definition of the filum terminale is a wonderfully clear one, provided by a friend of mine, Nancy Van Luven, a member of http://www.tetheredcord.com/:

“The filum terminale is like a thin elastic band, about 8 inches long. At the top, it is formed from one of the layers of tissue surrounding your spinal cord, and extends from the bottom of your spinal cord to the tip of your tail bone. The outside of the “elastic band” has a few nerve fibres sticking to it.

The filum terminale works as an anchor for the spinal cord. For people with normal anatomy, the filum stretches when they bend over to allow the spinal cord to move up in the spinal column and then goes back to normal length when the person straightens up and gently pulls the spinal cord back to its normal position.

When the filum is fat-filled, fibrous and tight, it will not allow the spinal cord to move up and down within the spinal column, and so the spinal cord and the nerves end up being stretched instead of the filum. In most people this causes nerve damage”.

Everybody has a filum terminale; it is a threadlike piece of tissue that connects the end of the spinal cord to the sacral end of the spinal canal in the pelvic area. In patients with a thickened filum (defined as more than 2 mm in diameter) [Yundt, 1997], the filum is shorter or lower-lying than normal and is thickened with fatty or fibrous tissue. This abnormality causes the filum to become relatively inelastic (a bit like a rope or cord, rather than an elastic band) and the spinal cord becomes tethered at an abnormally low level, thereby giving rise to the recognised signs and symptoms of a tethered spinal cord.

The usual cutaneous marker in 50% of patients is a deep, skin-covered dimple (closed dermal sinus tract) in the spinal midline, very low down on the back around the coccyx area. However thickened filums “may not always be attached to a sinus” [Ian Pople, 2002] and therefore any changes in the development of an apparently normal child’s feet, legs, back, bladder and bowel control should be investigated for an underlying thickened filum. The earlier a diagnosis is made may possibly prevent further irreversible neurological damage. “However, it is inevitable that in most children some deformity occurs even after an early detethering, except in those cases with purely a thickened filum presenting with pain, where the neurological outcome is generally better [Ian Pople, 2004].

A diagnosis of a deterioration in the condition of a spinal cord due to a thickened filum terminale is usually made after an MRI (3D scan) as well as taking account of painful physical symptoms. The symptoms of deterioration can include any of the following:

progressive scoliosis

muscle stiffness, weakness, or atrophy

intermittent on-again-off-again pain in the back of one or both legs and in the lower back

pain in a radicular distribution, elicited by a straight leg raising test which places further traction on the cord.

The operation to release the thickened filum is the simplest and least risky of untethering procedures as the filum has no neurological function and the surgery hold a 1-2% risk of causing neurological deterioration or damage. It involves a laminectomy at one or two levels in the lumbar or sacral spine to expose the site of the tether, and a division of the tight filum is made. The patient usually has to lie flat in hospital for about five days to prevent CSF leakage or damage to the incision site. S/he can take graduated gentle exercise as the wound heals and physical strength returns. The sciatica-like leg pain and severe spinal pain, characteristic of this type of tethered cord, usually reduces or disappears in most patients. Some of the post-operative pain can be attributed to being “a feature of released sensory tissue beginning to work after many years of being shut off by the tethering” [Ian Pople, 2002], and some patients continue to suffer chronic pain, varying in types and levels of intensity.

The success of the surgery can be measured when the cord can move in a normal manner, as the tension on it will have been released. A successful detethering will also halt further deterioration of the nerves affecting the lower extremities and of the bladder and bowel. Prior to surgery, the nerves of the cauda equina are stretched vertically like an elastic band. After a successful detethering these nerves are relaxed and lie, as they should do, at right angles to the filum and spinal cord.

I had this type of tethered cord, and I have undergone detethering surgery. Please go to my home page to follow my experiences and progress

Retethering

“A patient with a simple tight terminal filum usually experiences an uneventful postoperative course, and there is little chance of retethering” (M.R. Proctor and R.M. Scott, “Long Term Outcome for Patients with Split Cord Malformation”, Neurosurgery Focus, 10(1), Article 5, 2000. Two other articles were particularly informative about retethering of spinal cords post-surgery.

“Objective and Importance: The release of a tethered spinal cord by sectioning a thickened filum terminale is a straightforward surgical procedure that can prevent, arrest, or ameliorate neurological deficits. We recently recognized progressive neurological deterioration cause by filum retethering in two patients years after this procedure was performed. This sequela of a recurrent tethered cord after the sectioning of a filum terminale has not previously been described.

Clinical Presentation: Two female patients, each 13 years of age at presentation, had been previously operated on for tethered spinal cords secondary to fibrolipomatous (fatty) fila terminale. Both presented with bladder dysfunction and one with progressive paraparesis. MRIs revealed a low-lying conus medullaris and a sectioned filum with the proximal stump adherent to the posterior dura.

Intervention: Each patient underwent neurosurgical exploration of the previous site of sectioning, with the recognition of the retethered proximal stump of the filum terminale. After re-release of the fatty filum, the patient with only bladder dysfunction stabilized and a motor examination revealed normal results for the patient with progressive paraparesis.

Conclusion: Retethering of the spinal cord is a rare sequela (consequence of) [after] the sectioning of a tight filum terminale. The clinical presentation is typical for recurrent cord tethering and the radiographic findings are subtle. Careful surgical exploration should be offered for spinal cord untethering. Awareness of this rare and hitherto undescribed sequela is necessary for appropriate long-term management of tethered spinal cords cause by fatty filum terminale.”

“Objective: The purpose of this study was to describe the natural history of tethered cord in patients who have undergone meningomyelocele repair.

Methods: We performed a retrospective review of 45 patients with a history of neonatal meningomyelocele repair who consequently developed symptoms of tethered cord. Symptoms of tethered cord in this cohort consisted of the development of bladder spasticity or orthopedic foot deformity. None of these patients were treated with cord untethering; instead they were treated symptomatically.

Results: On follow-up, 40 (88.9%) of these patients subsequently required additional orthopedic or urological procedures because of further symptoms of tethered cord. The incidence of progression of tethered cord syndrome is 27.5, 40, and 60% at 1, 2, and 5 years respectively.

Conclusion: Although this study does not address the question whether cord untethering will prevent further symptom development, these results do provide a strong rationale for consideration of an untethering procedure in patients with repaired meningomyelocele at the time of the onset of symptoms of tethered cord.”

In another study, it was noted that “~10-16% of children with spina bifida are at risk of a secondary tethering where 87% of these are diagnosed by neuro-urological surveillance, and a further 4 out of 191 children were diagnosed with a secondary rethering because they developed a peripheral neurological deterioration in the lower extremities as detected by routine neurological examination” (Ilker, Y. et al) (see Information Pages)

At present there appears to be no guaranteed way to prevent retethering, although various methods are being used. Aliredjo et al [1999] support the use of a Gore-Tex membrane to prevent adhesions after cord detethering but other surgeons are experimenting with an anti-adhesion gel .

The risk of retethering can vary according to the patient’s age, the type, and the severity of the entire condition. In children the risk of cord retethering is approximately 20% “because the spinal canal in the baby is shallow and therefore postoperatively the neural contents are in direct contact with the posterior dura (back covering of the spinal cord) [Zide et al., 1995]. In adults who have been detethered, there may be a ~5-10% risk of the cord retethering.

Journal and research paper extracts

Below are some extracts of research papers from journals, relating to thickened filum terminale.

“The most common tethering lesions [in adults exhibiting symptoms of a tethered cord] were intradural lipoma and a short thickened filum terminale … the surgical outcome was gratifying in relation to pain and sensory-motor deficits but disappointing in the resolution of sphincter disorders” [Caruso et al, 1996].

In studies of patients with “tight filum terminale, split cord malformation and lipomyelomeningocele … long term surgical improvement was reported … 79% called the operation a long-term success; 75% believed they had significant postoperative improvement (and not just stabilization) in pain and/or neurological function” [Iskandar et al., 1998].

“The patients presenting with low back pain and sciatica responded to surgery better than those with sphincter problems” [Akay et al., 2000].

Urological aspects of tethered cords

“Adults with the tethered cord syndrome are less likely to have urodynamic or bladder function improvement after cord release and most often present with irreversible findings which rarely become worse after surgery. These patients need to have careful and continuous follow-up, including urodynamic studies, due to possible re-tethering with time” [Giddens et al., 1999].

In a group of patients with primary cord tethering “the most common preoperative urodynamic finding was hyperreflexia, which improved or resolved after untethering in 62.5% of the patients. Four adults also reported improved bladder sensation or decreased urgency”. In a second group of patients who had undergone a second detethering surgery “only 14% had improved symptoms of urinary control but 28% had improved lower extremity function”. The conclusion was that “urological symptoms and urodynamic patterns may be improved by early surgical intervention in patients with occult spinal dysraphism. However, untethering did not consistently benefit patients with secondary spinal cord tethering” [Fone et al., 1997].

In children with lower urinary tract dysfunctions “significant improvements can be achieved with a judiciously timed division of the tethered spinal cord” [Balkan et al., 2001].

“Changes in bladder-sphincter function after untethering are usually transient and often the result of partial denervation [mostly in patients with myelomeningocele and lipomyelomeningocele] … however the individual outcome cannot be predicted [Boemers et al., 1995].

Dermal sinus tract

This condition manifests itself as a small skin-lined tube (a fistula) found along the midline of the back, usually in the lumbar or sacral part of the spine, which extends through two (possibly damaged) laminae, through spinal cord coverings, and deep into the end of the spinal canal. The dermal sinus is usually attached to the spinal cord, thus causing tethering of the cord. It is caused when the neural tube fails to separate fully from the overlying ectoderm during weeks 3-5 of pregnancy. See Yamada (pp. 6-20) for detailed explanations of these processes.

Cutaneous markers may be any of the following:

collections of blood vessels just under the skin

abnormally placed tufts of hair

deep skin dimples

skin discoloration around a variously-sized skin opening

on examination, the existence of a fistula.

Surgery to correct this condition is generally required, due to the risk of spinal cord abscesses, the entry of bacteria through the tract with the increased risk of meningitis and the potential damage due to the tethering of the spinal cord. The surgery generally involves removing any portions of the sinus tract that connect with the spinal cord and covering the tract to reduce infection.

Diastematomyelia (also called split cord malformation).

This type of tethered cord occurs when the spinal cord is split in two longitudinally by a spur of bone or cartilage and is formed at approximately days 16/17 post-conception. Each half usually possesses its own dorsal and ventral nerve roots and is enclosed within its own dural sheath (cord covering). The two cords may reunite above and below the dividing structure. Diastematomyelia may be associated with bone abnormalities such as split or fused vertebrae, may also be seen with a short filum terminale, a tumour, or the tethering of nerve roots around the diastematomyelia. It is commonly located at the lower thoracic or upper lumbar areas of the back. It acts as a tethering process as it slows the normal growth of the spinal cord by preventing the upward migration of the cord.

Cutaneous features may include any of the following, depending on the level of tethering and the inclusion of other tethering factors:

Hypertrichosis, which is a patch of long silky hairs with a triangular outline, peculiar to 50-70% of cases of this condition

Neurological changes such as weakness, atrophy of muscles, gait changes, sensory changes or loss in legs and feet, and bowel and bladder disturbances

Some cases of diastematomyelia are initially asymptomatic and require careful monitoring. However, in many cases neurological deterioration occurs and therefore surgery is indicated. The standard surgery, which is described by Proctor and Scott is “the removal of the fibrous or bone septum, resection of any other local spinal cord attachments causing tethering, and exploration for associated tethering-related anomalies such as dorsal tethering bands or thick filum, which can be seen in the majority of SCM patients. Following the detethering procedure, the dura was closed posteriorly with or without placement of a patch graft … the patients were kept flat postoperatively for an average period of 72 hours, and were then allowed to progressively advance to full activity levels”. This releases the tethering of the cord and modest neurological improvement is reported.

Lipomyelomeningocele

This is the most severe form of tethered cord that is covered by skin, and accounts for 84% of occult spinal cord malformations. Adipose tissue collects in a defect of the spinal column, and the spinal cord, functioning nerve roots, conus and filum terminale become embedded in this pad of fat thereby tethering the spinal cord. This situation can compress the cord leading to possibly irreversible neurological damage and deterioration.

The cutaneous marker is obvious upon examination in the form of a non-symptomatic lump under the unbroken skin. The placement of this lipoma is usually in the lumbosacral region of the back.

Clinical features secondary to the lipoma may include

motor and sensory deficits

reflex changes

gait and stance abnormalities

bowel and bladder problems

musculo-skeletal problems.

These symptoms can cause progressive problems in adulthood after a possibly relatively symptom-free childhood, and surgery is usually required to prevent further neurological deterioration.

The operation to correct this condition consists of removing the fatty lipoma and thus detethering the spinal cord and its nerves. Some literature (found at http://nyneurosurgery.org/) indicates that surgeons detether this type of cord by using a laser to vaporise the water content in the fat, thus “melting” the lipoma and enabling its removal without injury to the neural structures around it.

One journal paper was very informative – “Recurrent Tethering: A Common Long-Term Problem after Lipomyelomeningocele Repair”, by A. Colak, I.F. Pollack, and A.L. Albright, Pediatric Neurosurgery, 29(4): October 1998.

They wanted to “determine the incidence and time course of symptomatic retethering in a control group of 94 patients … 20% of patients (19 people) reviewed required 28 subsequent operations for retethering. The median time between the initial procedure and reoperation for retethering was 52 months. The primary complaint of 12 patients was intractable low-back or leg pain, … progressive bowel and/or bladder dysfunction, deterioration of motor function and foot deformities … people with lipomas had a higher frequency of retethering rather than those with dorsal lesions … none of a variety of types of dural graft materials appeared to entirely prevent retethering. Following reoperation pain complaints resolved and many of the other symptoms improved partially or resolved completely”.

The researchers concluded that “symptomatic retethering is a common problem in children with lipomyelomeningoceles even after an adequate initial operation. To date, no type of graft material has been shown to entirely prevent this problem”.

Before surgical techniques were developed to detether lipomyelomeningoceles safely and effectively, patients with the condition often experienced considerable difficulties as both children and older adults. The following story illustrates how the condition can progress without childhood surgery. It also shows that lipomyelomeningocele can be improved by surgery, but that there is a greater risk that detethering surgery may have to be experienced more than once.

“In 1945 when I was born, little was known about spina bifida and tethered cord had never been heard of. There were also no shunts to prevent hydrocephalus. Surgeons simply closed the back and hoped for the best. My parents were told I was best left alone, as my back was covered by normal skin and I did learn to walk after a fashion. I grew up dealing with lack of enervation to my calf muscles, no sensation in the buttocks area and down the back of my legs, and increasingly deformed feet with hammer toes. I had no sensation to tell me my bladder was full, and I learned to use abdominal muscles to control both bladder and bowel. I fell often and couldn’t run, even burned the back of my leg sitting on a hot radiator. I wore corrective shoes which I did under protest and usually worked out how best to do something. If I fell or was hit on the lipoma I had tingling down my legs and more trouble walking.

By the time I was 40-ish I began to have severe pains in my hip and knees, but I was not referred to a neurologist as my doctor thought I had arthritis due to my compensated gait. After losing all bladder control I demanded a referral to a neuro-specialist and I finally found out about my condition. The MRI showed that the lipoma clearly entered the spinal column at L4, L5 and S1 and these vertebrae had no back to them at all. The lipoma was firmly attached to the end of the spinal cord.

Surgery to detether the cord took place when I was 52 and most of the lipoma was removed. My pain was instantly better. The following year, however, the symptoms gradually returned and now I have to use a wheelchair or motorised scooter to get around. My feet are also continuing to contract and so I may be facing a second detethering surgery to stabilise the condition.”

Urodynamics

Urodynamics refers to a group of procedures that are performed to examine voiding (urinating) disorders. The goal of the diagnosis and treatment of these disorders is to both protect the kidneys and keep the patient dry. Any procedure designed to provide information about a bladder problem can be called a urodynamic test. The type of test you take depends on your problem.

Most urodynamic testing focuses on the bladder’s ability to empty steadily and completely. It also can show whether or not the bladder is having abnormal contractions, which cause leakage. Your doctor will want to know whether you have difficulty starting a urine stream, how hard you have to strain to maintain it, whether the stream is interrupted, and whether any urine is left in your bladder when you are done. The urodynamic test is a precise measurement using sophisticated instruments.

Before the Test

You will need to take the antibiotic that has been provided. You will need to have a urine culture to make sure you do not have a urinary tract infection.

The test includes:

Uroflowmetry

A uroflowmeter automatically measures the amount of urine and the flow rate (how fast the urine comes out). This creates a graph that shows changes in flow rate from second to second so the doctor or nurse can see the peak flow rate and how many seconds it took to get there. This test will be abnormal if the bladder muscle is weak or urine flow is obstructed.

The volume of urine is divided by the time to see what your average flow rate is. For example, 330 ml of urine in 30 seconds mean that your average flow rate is 11 ml per second.

Postvoid residual

After you’ve finished urinating, you may still have some urine, usually only an ounce or two, remaining in your bladder. To measure this urine, called a post-void residual, the nurse may insert a catheter into your bladder, drain the urine and measure it. A post-void residual of more than 200 ml (about half a pint) is a clear sign of a problem. Even 100 ml, about half a cup, may require further testing.

Cystometry (cystometrogram – CMG)

A cystometrogram (CMG) measures how much your bladder can hold, how much pressure builds up inside your bladder as it stores urine, and how full it is when you feel the urge to urinate. The nurse will use a catheter to empty your bladder completely. Then a special smaller catheter with a pressure-measuring tube called a cystometer will be used to fill your bladder slowly with normal saline. Another catheter will be placed in the rectum to record pressure there as well. You will be asked how your bladder feels and when you feel the need to urinate. The volume of water and the bladder pressure will be recorded. You will be asked to cough or strain during this procedure. Involuntary bladder contractions can be identified.

Measurement of leak point pressure

While your bladder is being filled for the CMG, it suddenly may contract and squeeze some water out without warning. The cystometer will record the pressure at the time of the leak. This reading tells the doctor about the kind of bladder problem you have. You also may be asked to exhale while holding your nose and mouth closed to apply abdominal pressure to the bladder, or cough or shift positions. These actions help the doctor or nurse evaluate your sphincter muscles.

Pressure flow study

After the CMG, you will be asked to empty your bladder so that the catheter can measure the pressures required to urinate. This pressure flow study helps to identify bladder outlet obstruction that men may experience with prostate problems. Bladder outlet obstruction is less common in women but can occur with a fallen bladder or rarely after a surgical procedure for urinary incontinence. Some catheters can be used for both CMG and pressure flow studies.

Electromyography (measurement of nerve impulses)

During the urodynamics test, an electromyograph will be performed to measure nerve impulses. This test measures the muscle activity in the urethral sphincter using sensors placed on the skin near the urethra and rectum. Sometimes the sensors are on the urethral or rectal catheter. Muscle activity is recorded on a machine. The patterns of these impulses will show whether the messages sent to the bladder and urethra are coordinated correctly.

Afterward

You might have mild discomfort for a few hours after these tests. Drinking two 8-ounce glasses of water each hour for 2 hours should help. Ask your doctor whether or not you can take a warm bath. If not, you may be able to hold a warm, damp washcloth over the urethral opening to relieve the discomfort.

Your doctor may give you an antibiotic to take for 1 to 2 days to prevent an infection. If you have signs of infection, fever, chills or pain, call your doctor.

Results

For some of the more simple tests, you may get answers as the test is being done or right after it’s done. For others, it will take a few days. Your doctor will contact you with the answers.

Courtesy of National Kidney and Urologic Diseases Information Clearinghouse

What Happens In Human Spinal Cord Injuries?

Although the spinal cord is protected by the bony vertebrae of the spinal column, it can still be injured …with disastrous consequences. According to statistics gathered in 1996 by the National Institutes of Health, more than 10,000 Americans experience spinal cord injuries each year and more than 200,000 are living with permanent paralysis in their arms or legs.

People with spinal cord injuries can also lose sensation and — depending where along the spinal cord the injury occurs — control over critical body functions, including the ability to breathe. And because two-thirds of spinal cord injuries occur in people who are 30 years old or younger, the resulting disabilities can affect their entire adult lives.

Usually, injuries to the spinal cord injuries do not result in a cut through the cord; instead, they crush the thin, fibrous extensions of nerve cells that are surrounded by the vertebrae. These extensions are called axons, the long, thin strings of nerve cell cytoplasm that carry electrical signals up and down the spinal cord. The axons of nerve cells with similar functions run in groups or pathways. Some carry sensory information upward to the brain; others run downward from the brain to control the body’s movements. An injury to the spinal cord can damage a few or many of these pathways. Nevertheless, a person can often recover some functions that were lost because of the initial injury.

The damage that occurs to spinal cord axons within the first few hours after injury is complex and it occurs in stages. The normal blood flow is disrupted, which causes oxygen deprivation to some of the tissues of the spinal cord. Bleeding into the injured area leads to swelling, which can further compress and damage spinal cord axons. The chemical environment becomes destructive, due primarily to the release of highly reactive molecules known as free radicals. These negatively charged ions can break up cell membranes, thus killing cells that were not injured initially. Blood cells called macrophages that invade the site of injury to clean up debris may also damage uninjured tissue. Non-neuronal cells including astrocytes may divide too often, forming a scar that impedes the regrowth of injured nerve cell axons.

Micrograph of the spinal cord of an adult rat. As in the human patient, a central cavern (dark) replaces the damaged tissue. A group of descending fibers (white matter) that normally control voluntary movement — called the corticospinal tract — ends at the wall of the cavern, indicating that the cavern and its associated scar tissue act as a barrier to regeneration.

A magnetic resonance image (MRI) of the cervical spinal cord of a paraplegic patient showing a cavern (dark area) that has formed at the site of injury. The spinal cord is crushed, not severed, as seen by the continuity of the white matter.

The early events that follow a spinal cord injury can lead to other kinds of damage later on. Within weeks or months, cysts often form at the site of injury and fill with cerebrospinal fluid, the clear, watery fluid that surrounds the brain and spinal cord. Typically, scar tissue develops around the cysts, creating permanent cavities that can elongate and further damage nerve cells. Also, nerve cell axons that were not damaged initially often lose their myelin, a white, fatty sheath that normally surrounds groups of axons and enhances the speed of nerve impulses.

Over time, these and other events can contribute to more tissue degeneration and a greater loss of function. Scientists are trying to understand how this complex series of disruptive events occurs so they can find ways to prevent and treat it. They are also trying to identify treatments that will enhance some of the normal — but often limited — kinds of recovery that can occur after a spinal cord injury.

Another complication in spinal cord injury stems from the variety of nerve fibers and cell types that make up the tissue. In the spinal cord, axons run in bundles or pathways up and down the cord. The downward or descending pathways from the brain to the spinal cord carry nerve signals that control voluntary movements. The upward or ascending pathways carry sensory information — about touch, temperature, pain, and body position — from the entire body to the brain. Researchers believe that the ascending and descending pathways, as well as different groups of nerve cells (also called neurons) that lie entirely within the spinal cord, may require individualized treatments to regenerate and regain their functions.

“Do the descending motor pathways from the brain into the spinal cord need the same things [for recovery] as sensory fibers that go from the spinal cord to the brain?” asks Barbara Bregman, a neuroscientist in the department of anatomy and cell biology at Georgetown University in Washington, D.C. “It is important to know what the cells need and when they need it.”

For example, if scientists are going to be able to devise ways to repair damaged spinal cord tissue, they may need to use special combinations of nourishing proteins — called neurotrophic factors — to help damaged axons to regrow and regain some function. The damaged cells may also require a specific environment in which to recover. So researchers study the chemical composition of the non-cellular material — the extracellular matrix — that surrounds healthy neurons in the spinal cord and in the peripheral nervous system that serves the rest of the body. Additionally, damaged spinal cord neurons may require the presence — or even the absence — of different kinds of non-neuronal cells for regrowth and functional recovery.

Although scientists are beginning to understand the cellular and molecular events that occur after spinal cord injury, one question continues to dominate the research: Why don’t the brain and spinal cord repair themselves?

What is an Epidural Steroid Injection?

Epidural Steroid Injection is an injection of long lasting steroid (cortisone) in the Epidural space – that is the area surrounding the spinal cord and the nerves coming out of it.

What is the purpose of it?

The steroid injected reduces the inflammation and/or swelling of nerves in the Epidural space. This may in turn reduce pain, tingling & numbness and other symptoms caused by nerve inflammation / irritation or swelling.

How long does the injection take?

The actual injection takes only a few minutes.

What is actually injected?

The injection consists of a mixture of local anesthetic (like lidocaine or bupivacaine) and the steroid medication (triamcinolone – Aristocort® or methylprednisolone – Depo-medrol®, Celestone-Soluspan).

Will the injection hurt?

The procedure involves inserting a needle through skin and deeper tissues (like a “tetanus shot”). So, there is some discomfort involved. However, we numb the skin and deeper tissues with a local anesthetic using a very thin needle prior to inserting the Epidural needle. Also, the tissues in the midline have less nerve supply, so usually you feel strong pressure and not much pain. Most of the patients also receive intravenous sedation and analgesia, which makes the procedure easy to tolerate.

Will I be “put out” for this procedure?

No. This procedure is done under local anesthesia. Most of the patients also receive intravenous sedation and analgesia, which makes the procedure easy to tolerate. The amount of sedation given generally depends upon the patient tolerance.

How is the injection performed?

It is done either with the patient sitting up or on the side, or on your stomach. The patients are monitored with EKG, blood pressure cuff and blood oxygen monitoring device. The skin in the back is cleaned with antiseptic solution and then the injection is carried out. After the injection, you are placed on your back or on your side.

What should I expect after the injection?

Immediately after the injection, you may feel your legs slightly heavy and may be numb. Also, you may notice that your pain may be gone or quite less. This is due to the local anesthetic injected. This will last only for a few hours. Your pain will return and you may have a “sore back” for a day or two. This is due to the mechanical process of needle insertion as well as initial irritation form the steroid itself. You should start noticing pain relief starting the 3rd day or so.

What should I do after the procedure?

You should have a ride home. We advise the patients to take it easy for a day or so after the procedure. Perform the activities as tolerated by you.

Can I go back to work the next day?

You should be able to unless the procedure was complicated. Usually you will feel some back pain or have a “sore back” only.

How long does the effect of the medication last?

The immediate effect is usually from the local anesthetic injected. This wears off in a few hours. The cortisone starts working in about 3 to 5 days and its effect can last for several days to a few months.

How many injections do I need to have?

If the first injection does not relieve your symptoms in about a week to two weeks, you may be recommended to have one more injection. Similarly If the second injection does not relieve your symptoms in about a week to two weeks, you may be recommended to have a third injection.

Can I have more than three injections?

In a six month period, we generally do not perform more than three injections. This is because the medication injected lasts for about six months. If three injections have not helped you much, it is very unlikely that you will get nay further benefit from more injections. Also, giving more injections will increase the likelihood of side effects from cortisone.

Will the Epidural Steroid Injection help me?

It is very difficult to predict if the injection will indeed help you or not. Generally speaking, the patients who have “radicular symptoms” (like sciatica) respond better to the injections than the patients who have only back pain. Similarly, the patients with a recent onset of pain may respond much better than the ones with a long standing pain. Also, the patients with back pain mainly due to bony abnormality may not respond adequately.

What are the risks and side effects?

Generally speaking, this procedure is safe. However, with any procedure there are risks, side effects, and possibility of complications. The most common side effect is pain – which is temporary. The other risk involve spinal puncture with headaches, infection, bleeding inside the Epidural space with nerve damage, worsening of symptoms etc. The other risks are related to the side effects of cortisone: These include weight gain, increase in blood sugar (mainly in diabetics), water retention, suppression of body’s own natural production of cortisone etc.

Who should not have this injection?

If you are allergic to any of the medications to be injected, if you are on a blood thinning medication (e.g. Coumadin, Plavix), or if you have an active infection going on, you should not have the injection.

What is a Myelogram?

A myelogram is a special x-ray examination to study your spinal canal, spinal cord and the area surrounding it called the subarachnoid space. The procedure involves the injection of contrast material or dye into your spinal canal. This contrast material is an iodinated contrast medium similar to what is injected for a study of the kidneys called an intravenous pyelogram (IVP), and is often injected for CT scans, cardiac catheterizations and angiograms for enhanced visualization.

Note: If you have had a previous allergic reaction to iodinated contrast material, please notify your physician so that the proper steroid preparation can be ordered before your scheduled myelogram.

A myelogram can identify abnormalities of the spinal cord, the spinal canal within which it sits, and the spinal nerve roots connected to it. Myelography is often performed when other exams such as computerized tomography (CT) scans or magnetic resonance imaging (MRI) have not provided enough information for an accurate diagnosis to be made.

How Do I Prepare for a Myelogram?

No food should be eaten two (2) hours prior to your myelogram, but fluids are permitted.

Please let your physicians know about any allergies to food or medications in advance. Also, please notify your physician if you are taking any blood thinning medications such as:

Aspirin

Coumadin

Heparin

Plavix

Lovenox

In most cases, such medications will need to be discontinued for a period of time before your procedure according to your physician’s instructions.

If you are taking any major tranquilizers, please inform your physician, as some of them may need to be discontinued two days prior to the procedure and restarted one day after the procedure.

Although myelograms are performed on an outpatient basis, we ask that you do NOT drive yourself to the Clinic on the day of your myelogram appointment. Arrangements must be made for someone to drive you TO and FROM your myelogram appointment. Your procedure may be canceled if transportation arrangements are not made in advance.

If you have had MRI or CT films of the spine at another facility, please bring them with you on the day of the myelogram procedure.

What Can I Expect During the Procedure?

When you arrive in the Diagnostic Radiology Department you will be asked to change into a hospital gown, with the opening at the back. At this time you should urinate so you will be comfortable during your myelographic study. Please notify the technologist if you have a history of allergies or seizure disorder. Women in their childbearing years will also be asked about the possibility of pregnancy. If there is any possibility that you may be pregnant, please inform your doctor or the technologist prior to the examination. If you have a fever, call first as it may be necessary to postpone the procedure.

When the examination begins, you will likely be positioned face down on a special x-ray table for the myelographic procedure. This table will be tilted up or down as necessary during the procedure. At different times during the procedure you may be asked to lie on your side or back as well.

Depending on the area to be studied, either your back or neck will be washed with a soapy iodine solution. That area will then be covered by a sterile drape. After injecting a numbing medication (xylocaine) into your neck or back, the radiologist will place a needle into your spinal canal using x-ray guidance, inject the contrast material, and take a series of X-rays of the area in question.

The myelogram procedure takes approximately thirty to sixty minutes to complete, but you can expect to remain in the recovery area for a period of time after your study is finished.

What Can I Expect After my Procedure?
When your myelographic study is complete you will be put on a stretcher in either a semi-upright or flat position. Usually a CT scan will be performed after the myelogram. You will be sent to a recovery area for approximately two (2) hours where a nurse will monitor your progress. You may get up to use the bathroom, but otherwise you should stay in bed and remain on your back for the full two (2) hours. You will be given something to eat and encouraged to drink fluids. Drinking fluids helps eliminate the possibility of side effects, such as headaches, nausea and vomiting. If a headache, backache, or nausea should occur while you are in the recovery area, let the nurse know immediately. Medications are available to help make you more comfortable

MENINGEAL or perineural (Tarlov) cysts are meningeal dilations of the posterior spinal nerve root sheath most commonly seen at the sacral level (1). Tarlov cysts can cause progressive radiculopathy, pelvic pain, sphincter dysfunction, and buttock and lower extremity pain. They are most commonly diagnosed with lumbosacral magnetic resonance (MR) imaging and can often be demonstrated at computed tomographic (CT) myelography to communicate with the spinal subarachnoid space. These cysts may be large and expand the spinal canal,
sometimes causing erosion of the overlying bone. Numerous treatment approaches for symptomatic Tarlov cyst have been described, including surgical cyst fenestration, partial cyst wall resection, and myofascial flap repair and closure (2–11). More recently, a less invasive, percutaneous approach with a single needle aspiration technique has been reported (5,7). In general, this procedure consists of three stages: (a) cyst entry and aspiration, (b) contrast medium injection to ensure there is no wide connection between the cyst and thecal sac, and (c) tissue adhesive injection.
We have treated numerous patients with a single-needle aspiration technique. A substantial limitation of this approach is the severe intraprocedural pain that develops during aspiration, which is thought to be related to negative pressure retraction on the dura. We therefore developed a two needle technique in which one needle is positioned at the apex of the cyst and a second one is positioned in its lowest portion to allow equilibration of pressure within the cyst during aspiration and obliteration.